The haemodynamic effect of intravenous flecainide acetate in patients with coronary artery disease.

Serruys, Patrick W.; Vanhaleweyk, G.; Brand, Marcel van den; Verdouw, Pieter D.; Lubsen, J; Hugenholtz, Paul G.

doi:10.1111/j.1365-2125.1983.tb02143.x

Cited by 33 publications

(11 citation statements)

References 13 publications

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“…On the other hand, after intrave nous administration of 2 mg/kg fiecainide over a 10-min period in coronary artery dis ease patients, a negative effect on left ventric ular pressure derived variables was demon strated in our laboratory under resting condi tions and during atrial pacing stress. In view of these findings, the use of flecainide in patients with cardiac dysfunction should be further evaluated [28]. In conclusion, our study confirms the anliarrhythmic potential of flecainide acetate seen in animal experi ments and in other recent clinical studies [5][6][7][8][9][10][11][12].…”

Section: Discussionsupporting

confidence: 77%

Oral Flecainide for Suppression of Ventricular Arrhythmias

Vanhaleweyk¹,

Balakumaran²,

Lubsen³

et al. 1984

Cardiology

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The efficacy and safety of oral flecainide for treatment of ventricular arrhythmias were assessed during a 3-day period in patients with various cardiac diseases. Of 11 patients who received a low dose of flecainide (median daily dose 240 mg), only 4 responded with 90% or greater reduction in premature ventricular complex frequency. Ventricular tachycardia could not be suppressed. During treatment no electrocardiographic changes occurred. 14 of the 19 patients who received a high dose of flecainide (median daily dose 480 mg), demonstrated a 90% or greater reduction in premature ventricular complexes, and ventricular tachycardia did not recur during treatment in 7 out of 9 patients. However, PQ, QRS, and QTc intervals were significantly increased. In general, flecainide was well tolerated and drug administration did not have to be discontinued because of side effects. Flecainide acetate treatment, with a median dose of 480 mg daily, appears to be highly effective for suppressing complex ventricular arrhythmias.

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Section: Discussionsupporting

confidence: 77%

Oral Flecainide for Suppression of Ventricular Arrhythmias

Vanhaleweyk¹,

Balakumaran²,

Lubsen³

et al. 1984

Cardiology

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“…These data are in general agreement with other reports of the effects of these drugs administered intravenously in acute myocardial infarction and stable coronary artery disease (Miller et al, 1973;Beck et al, 1978;Burton et al, 1976;Rahimtoola etal., 1971;Schumacher etal., 1968;Grossman et al, 1969;Cameron et al, 1984;Hulting et al, 1976, Kotter et al, 1980 , , Serruys et al, 1983Josephson et al, 1984). Unfortunately the lack of standardisation of experimental protocols between these various studies makes direct comparisons problematical.…”

Section: Discussionmentioning

confidence: 99%

“…Although the individual haemodynamic effects of many anti-arrhythmics have been well characterised (Grossman et al, 1969;Miller et al, 1973;Hulting & Rosenhamer, 1976;Kotter et al, 1980;Serruys et al, 1983;Josephson et al, 1984), comparison of their actions is more difficult to assess. This stems from their circulatory assessment in independent laboratories with differing administration regimens, dosages and methodology.…”

Section: Introductionmentioning

confidence: 99%

Comparative haemodynamic effects of intravenous lignocaine, disopyramide and flecainide in uncomplicated acute myocardial infarction.

Silke¹,

Frais²,

Verma³

et al. 1986

Brit J Clinical Pharma

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A prospective study evaluated the comparative haemodynamic effects of three Class I antiarrhythmics (lignocaine Class 1B, disopyramide Class 1A and flecainide Class 1C) in 30 patients with uncomplicated acute myocardial infarction. Three groups, each of 10 patients, were allocated to lignocaine (Group I) 1.5 mg kg‐1 i.v. loading dose over 10 min followed by infusion at 3 mg kg‐1 h‐1, disopyramide (Group II) or flecainide (Group III), both administered as a 1.0 mg kg‐1 i.v. loading bolus over 10 min followed by a 1.6 mg kg‐1 h‐1 infusion for 120 min. The plasma levels of each drug were in the described therapeutic range. Lignocaine decreased cardiac index (‐0.3 l min‐1 m‐2 (9%); P less than 0.05) and stroke volume index (‐5 ml m‐2 (11%); P less than 0.01). Systemic blood pressure, heart rate and systemic vascular resistance index were unchanged. There was a small increase (+3 mm Hg (30%); P less than 0.01) in pulmonary artery occluded pressure (PAOP). Both disopyramide and flecainide increased systemic blood pressure; the maximum increases for mean blood pressure were +10 mm Hg (11%) and +4 mm Hg (4%) respectively. Both drugs reduced cardiac index (‐0.5 l min‐1 m‐2 (16%): −0.4 l min‐1 m‐2 (11%)) and stroke volume index (‐11 ml m‐2 (25%): −5 ml m‐2 (11%)). There were increases in heart rate (+13: +5 beats min‐1) pulmonary artery occluded pressure (+2: +3 mm Hg) and systemic vascular resistance index (+696: +275 dyn s cm‐5 m2).(ABSTRACT TRUNCATED AT 250 WORDS)

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“…In fact, flecainide prolonged the PR interval of the ECG (Somberg & Tepper, 1986), depressed cardiac contractility both in vitro (Schulze & Knops, 1982) and in vivo (Serruys et al, 1983;Josephson et al, 1984) and inhibited the slow action potentials elicited by isoprenaline in ventricular muscle fibres partially depolarized with high K (Schulze & Knops, 1982). However, and even when the cardiac and haemodynamic effects of flecainide are well established (Josephson et al, 1984;Holmes & Heel, 1985;Silke et al, 1986), little is known about its direct action on peripheral blood vessels and the calcium antagonistic properties of flecainide.…”

Section: Introductionmentioning

confidence: 99%

Effects of flecainide on isolated vascular smooth muscles of rat

Pérez‐Vizcaíno

Ding

Tamargo

1991

British J Pharmacology

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1 The inhibitory effects of flecainide were studied on contractile responses in rat isolated aortae and caudal artery and on spontaneous mechanical activity in portal vein segments.2 In rat isolated aorta flecainide, 1O-6m-5 x 10-0M, inhibited in a dose-dependent manner the contractile responses induced by high K (80mM) and noradrenaline (NA, 10-M). These inhibitory actions were observed when flecainide was added before or after the induced contractions and were similar in aortae with or without endothelium. 3 Contractile responses induced by addition of Ca to Ca-free high-K solution were also dosedependently inhibited by flecainide (IC50 = 2.5 + 0.3 x 10 -M). Moreover, flecainide inhibited the contractile responses elicited by NA in rings incubated in Ca-free solution.4 Flecainide also inhibited the spontaneous mechanical activity in portal vein segments (ICj0 = 6.5 + 0.9 x 1O 5M).5 Flecainide, 10-4M, inhibited 45Ca uptake stimulated by high K or NA without altering 45Ca uptake in resting aortae. 6 These results indicated that in rat isolated aortae, caudal arteries and portal veins, flecainide inhibited Ca entry through voltage-operated channels and NA-induced Ca uptake as well as Ca release from intracellular stores, thus decreasing the availability of intracellular free Ca required for vascular smooth muscle contraction.

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The haemodynamic effect of intravenous flecainide acetate in patients with coronary artery disease.

Cited by 33 publications

References 13 publications

Oral Flecainide for Suppression of Ventricular Arrhythmias

Oral Flecainide for Suppression of Ventricular Arrhythmias

Comparative haemodynamic effects of intravenous lignocaine, disopyramide and flecainide in uncomplicated acute myocardial infarction.

Effects of flecainide on isolated vascular smooth muscles of rat

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